SP-A enhances viral clearance and inhibits inflammation after pulmonary adenoviral infection

Surfactant protein A (SP-A) is a member of the collectin family of host def ense molecules expressed primarily in the epithelial cells of the lung. To determine the role of SP-A in pulmonary adenoviral infection, SP-A-deficien t (SP-A -/-) mice were intratracheally infected with a replication-deficien t recombinant adenovirus, Av1Luc1. Lung inflammation was markedly increased in SP-A -/- compared with SP-A +/+mice and was associated with increased h emorrhage and epithelial cell injury. Polymorphonuclear cells in bronchoalv eolar lavage fluid (BALF) were increased in SP-A -/- mice after administrat ion of adenovirus. Coadministration of adenovirus and purified human SP-A a meliorated adenoviral-induced lung inflammation in SP-A -/- mice. Concentra tions of tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-6, and I L-1 beta were increased in BALF of SP-A -/- mice. Likewise, TNF-alpha, IL-6 , macrophage inflammatory protein (MIP)-1 alpha, monocyte chemotactic prote in-1, and MIP-2 mRNAs were increased in lung homogenates from SP-A -/- mice 6 and 24 h after viral administration. Clearance of adenoviral DNA from th e lung and uptake of fluorescent-labeled adenovirus by alveolar macrophages were decreased in SP-A -/- mice. SP-A enhances viral clearance and inhibit s lung inflammation during pulmonary adenoviral infection,providing support for the importance of SP-A in antiviral host defense.